Hypertension was induced in Sprague-Dawley and Wistar rats by irregular foot shocks combined with a buzzing noise for 2 h twice a day for 1–2 weeks. The plasma catecholamine, cortico-sterone, angiotensin II, glucose and lipids were found to increase in parallel. The acetylcholine (ACh) and choline acetyltransferase in rostral ventrolateral medulla (rVLM) increased markedly. Microinjection of ACh or cholinergic agonists into rVLM induced a pressor effect, and microinjection of M receptor blockers had a depressor effect. Electrophysiological studies showed that the stress-induced hypertension was closely related to the activation of a cholinergic system in rVLM. Microinjection of corticoids into rVLM had led to a pressor response which could be blocked by Ru38486, spironolactone, cholinergic blockers or verapamil. Microinjection of morphine and µ- or δ-receptor agonists into rVLM caused bradycardia and a reduction of arterial pressure that could be blocked by naloxone.
The mesolimbic dopamine system is important for reward‐oriented behaviours, such as drinking and eating. However, the precise involvement of dopaminergic neurons and dopamine receptors in water drinking behaviour remains unclear. Here, we generated triple transgenic mice harbouring Slc6a3(DAT)‐icre/ERT2, Camk2a‐loxP‐STOP‐loxP‐tetracycline transactivator and tetO‐tetanus toxin constructs, in which the release of dopamine is blocked by tetanus toxin. These mice, referred to as dopamine secretion interference mice, had reduced dopamine secretion in the striatum (61.4%) and the nucleus accumbens (54.5%). They showed adequate limb strength and food consumption, similarly to control mice, but exhibited motor control impairment in a challenging rotarod test. Dopamine secretion interference mice made fewer licks and had fewer bursts than control mice during a licking test under thirsty conditions. To elucidate the influence of dopamine receptors in the altered drinking behaviour, a dopamine D1 or D2/D3 receptor agonist (A68930 or ropinirole, respectively) was administered prior to the licking microstructure analysis. Treatment with the D1 agonist restored the total number of licks but not the burst number in dopamine secretion interference mice. By contrast, the D2/3 agonist impeded water drinking behaviour in both transgenic and control mice. The present findings indicate that D1 receptor activation partially ameliorates the altered drinking behaviour of the dopamine secretion interference mice and suggest that D1 receptor activity impacts drinking under thirsty conditions.
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